The research objective is to elucidate the molecular basis of the process by which lung phagocytes ingest objects, the principal mechanism by which these cells defend human hosts against pulmonary infection. The motor aspects of this basic physiology phenomenon will be studied by attempting a complete characterization of contractile proteins from rabbit lung macrophages. Particular attention will be focussed on the properties of a high molecular weight actin-binding protein believed to regulate the state of actin in non-muscle cells and a potential key control point in the mechanism of cell surface to cytoplasm communication that occurs in phagocytosis, cell locomotion and in exocytosis of enzymes potentially toxic to the lung. The interaction of this protein with actin and its possible modification by other cellular agents will be studied with new assays for actin cross-linking. The control of lung macrophage actomyosin interaction will also be studied. The mechanism of action of a widely used drug, cytochalasin B, will be investigated.